An Atlas of Gas Poisoning UK 1918

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AS OF

POISONING









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For official use only)

QoMEDICAL RESEARCH fetJMMlTTCE

AN ATLASOF

GAS POISONING

1918



IQ

G1

Tiir Medical Research Committee have made the n. .

ments for the preparation and reproduction of the drawings shown in

this Atlas. The Atlas is printed for distribution in si/< uniform with

tlu series of Reports issued by the Chemical Warfare M

Committee with the sanction of the Director-General A.M.S. and of

the Controller of the Chemical Warfare Department, Minist

Munitions. The arrangements have been facilitated by the co-opera-

tion of the American Red Cross Society, who have undertaken to

provide part of the present issue of this Atlas for official distribution

in the American Army Medical Service.

The following Reports of the Chemical Warfare Medical Committee

have already been issued :

No. i. Notes on the Pathology and Treatment of the Effects of

Pulmonary Irritant Gases. (March, 1918.)

No. 2. The Histological Effects produced by Gas Poisoning and

their Significance. (April, 1918.)

No. 3. The Symptoms and Treatment of the Late Kfteets oi

Poisoning. (April, 1918.)

No. 4. Polycythaemia after Gas Poisoning and the Effect of Oxvg< n

Administration in the Treatment of Chronic Cases. (April, 1918.)

No. 5. The Reflex Restriction of Respiration after Gas Poisoning

(April, 1918.)

No. 6. Investigations into the Reaction of the Blood after Gas

Poisoning, and the Results of the Administration of Saline and other

Substances. The Effects of Bleeding and of the Injection of Calcium

Chloride. (April, 1918.)

No.7. Changes observed in the Heart and Circulation and the

general After-Effects of Irritant Gas Poisoning. (April, 1918.)

No. 8. Reports on Fatal Cases of Poisoning, (i.) Ethyl i<d<>-

acetate (Jnm\ 1918).



AN ATLASOF

GAS POISONINGTHE'SE drawings have been reproduced by the per-

mission of the Director-General of Medical Services,

B. E. F., and they are presented as a supplement to the

official memoranda on the Nature and Treatment of

Gas Poisoning that have already been issued by

General Headquarters to Medical Officers.

The drawings illustrate "only the chief features in the

pathology of the lesions produced by Enemy Gas, and

the primary aim of their distribution is that of general

instruction for Officers who are not already familiar

with the subject by experience in the field.

The copyright of all these drawings is reserved and

the contents of the Atlas must be regarded as con-

fidential and not to be communicated to the press.

B. E. F. FRANCE.

AUGUST i, 1918.





GENERAL INTRODUCTION

OUT of all the various substances used by the Enemy in Gas

Warfare only two have been chosen for illustration of tlirir

effects in this Atlas. They are Phosgene (COC12),and Di-chlor-

ethyl-sulphide, (QH4C1).S, or

'

Mustard Gas'.Phosgene is the chief of all the many gasses and liquids

that are used for their effects as pulmonary irritants. Chlorine

belongs to this group and was the first Poison Gas used by the

Germans in April 1915, but it has long since been superseded

by more effective chemical substances. The pulmonary irritants

are inhaled as gasses or vapours. They may cause some water-

ing of the eyes, but the chief effect noticed at once is a catching

of the breath or a choking sensation so that the chest feels

gripped and incapable of free respiration. Coughing and

vomiting may follow, and then after a delay of time varying

from a few minutes to several hours an inflammatory reaction

appears in the lungs themselves, with the development of an

acute oedema that may commence insidiously and yet progress

so rapidly as soon to be an immediate menace to life itself.

The alveoli fill with oedema fluid, which then rises into the

bronchial tubes and may appear in a most abundant expectorationof thin frothy fluid. Aeration of the blood is seriously interfered

with, because the air sacs are either drowned with oedema fluid

or burst by the efforts of coughing. Moreover the actual

circulation through the lungs is embarrassed, both by the

pressure of the oedema fluid on the capillary vessels and by

the local thrombosis that occurs in many places in the smaller

lung vessels. The blood itself is concentrated by the loss of serum

so that the count may rise to even eight or nine million red

corpuscles to the cu. mm. and this change probably adds to the

difficulties of the circulation.

The gassed man can no longer get the oxygen that he wants,

and he either dies in obvious asphyxia with progressive

circulatory failure, or he collapses as the result of sonic muscular

effort that suddenly makes a greater call for oxygen and so reveal.s



the deficiency of the supply. Death is the result simply of this

inflammatory oedema of the lung, and it occurs chiefly in the first

and secondday

after

exposureto

Phosgene.A few cases

maychance to develop secondary bacterial infections of the lungs

and to succumb to a later broncho-pneumonia, but they are

relatively rare.

The main clinical features of acute Phosgene poisoning maytherefore be summarized as follows :

(i) Catching of the breath, choking, and coughing immediately

on exposure to the gas.

(ii) Inability to expand the chest in a full breath after removal

from the poisoned air.

(iii) Vomiting, hurried shallow respiration, and sometimes

coughing with an abundant expectoration, follow. Pain is felt

behind the sternum and across the lower part of the chest. Fine

rales are heard in the axillae and over the back.

(iv) Cyanosis next appears, in association either with a full

venous congestion or with the pallid face of circulatory failure.

The development of these dangerous symptoms may occur after

many hours' delay, and sometimes with unexpected rapidity in

an apparently slight case as the result of muscular effort.

(v) Death, which may or may not be preceded by mild delirium

or unconsciousness, rarely occurs after the first or second day.

Di-chlor-ethyl-sulphide is spoken of as being a vesicant. It

may exert its irritant action either as a vapour in low concentra-

tion in the air orby

direct contact fromsplashes

of theliquid.

The liquid or vapour clings to the clothing of men exposed to

Yellow Cross shells, and thus slowly exerts its continuously

irritant action on their bodies.

No irritant effect at all is felt on first exposure, whatever the

concentration may be, but after a delay of about two to six hours

the skin and mucous membranes begin to react with a progressive

inflammation that may result in local necrosis and desquamationof these

covering membranes. Thereis

intense conjunctivitis ;

the skin turns an angry red, and this erythema is soon followed

by skin blistering here and there over the face and body. The

passage of the vapour down the respiratory tract may cause such

severe injury to the lining mucous membranes of the trachea and

bronchioles that they are eventually destroyedand sloughed away.Bacterial infection then seizes upon these raw surfaces, and the

patient may die from secondary septic broncho-pneumonia.



Death is never the direct result of the action of the poisonous

vapour. From the 2nd day onward through the first and second

weekseverely

affected menmay die,

butonly

as the result of

secondary bacterial infection. This poison therefore differs

entirely from the lung irritants such as Phosgene, which kill

directly and speedily b}^ flooding the lungs with oedema fluid.

The main features of poisoning from Mustard Gas may be

resumed as follows :

(i) Delay of the irritant effect for at 'least two to three hours,

and then a comparatively slow development of the various

inflammatory reactions.

(ii) Vomiting, and a sense of burning in the eyes, with

discomfort in the throat, hoarse cough, and some retro-sternal

pain.

(iii)Intense conjunctivitis that temporarily 'blinds' the man.

(iv) Burning of the exposed skin surfaces and of the moist areas

in the axillae and groin, followed by blistering, excoriation, and

brown staining.

(v) Inflammatory necrosis of the mucous membrane of the

trachea and bronchi, with the secondary development of infec-

tive bronchitis or septic broncho-pneumonia.

(vi) Death is relatively uncommon : it occurs later than the first

day and only as the result of septic complications.



LIST OF PLATES

No.

I. Microscopic section of human lung from phosgene shell

poisoning.

Death at the nineteenth hour after gassing.

II. Blue type of asphyxia from phosgene poisoning, with

intense venous congestion.

III. Pallid type of asphyxia from phosgene poisoning, with

circulatory failure.

IV. Gangrene of foot caused by vascular thrombosis from

chlorine poisoning.

V. Erythema of skin from general exposure to the vapour of

Yellow Cross substance.

VI. Blistering of buttocks by mustard gas.

VII. Burning of scrotum and penis by mustard gas.

VIII. Brown staining from mustard gas.

IX. Ulceration of trachea by mustard gas.

X. Microscopic section of human lung from mustard gas

poisoning, with death at end of second day (40 hours).

XI A. Severely burned eye in the acute stage.

X!B. Slightly later stage of acute burning.

XI IA. Stage of resolution after severe burning.

Xlle. Late stage of resolution.

XI 1 1 A. Drawing of the cornea in the acute stage of severe burning.

XI I IB. Drawing of cornea in the stage of resolution after severe

burning.





PLATE NO. 1

Microscopic section of human lung from phosgene shell

poisoning. Death at the nineteenth hour after gassing.

The piece of lung shown is almost entirely useless for aeration of

the blood. Most of the pulmonary alveoli are filled with oedema

fluid, and the walls of the air-sacs are burst asunder in many places.

The rounded edges of these torn walls can be recognized both in theareas of emphysema and in the parts that are flooded with oedema

fluid. The bronchus also is filled with oedema fluid, but it should

be noted that its lining epithelium is intact and pus cells have not

accumulated in the secretion. The blood vessels of the alveolar net-

work are congested ;and intravascular thrombosis is frequently found

in these smaller vessels, though it is not actually shown in the area of

this section.

The main changes in the lung are :

Congestion, and occasional thrombosis, of the network of pul-

monary blood vessels.

Abundant outpouring of inflammatory oedema fluid both into

the tissues and into the air spaces of the alveoli and bronchi.

Disruptive emphysema of the weakened lung tissue.

The result of these changes is that the blood circulation through the

lungs is impeded, and the respiratory exchange of gasses between the

blood and the air in the lung is seriously diminished. The gassedman is in danger of death by asphyxia so long as his lung is drowned

in oedema fluid.

From the third day onwards the oedema fluid is reabsorbed or

expectorated, and the lung soon resumes its functions. Broncho-

pneumonic complications may develop from secondary infections, but

they are not very common.

The recovery of the lung, even after severe gassing appears to be

functionally good. In the earlier stages of convalescence there maystill be signs of persisting oxygen want, so that tachycardia with

excessively rapid respiration is the result of even slight physical effort.

Later these disabilities vanish. The microscopic examination of lungs

in these stages of recovery has not been made.









PLATE NO. II

Blue type of asphyxia from phosgene poisoning, with

intense venous congestion.

History of case. Drawing made early on second day after gassing ;

when there was copious frothy sputum, frequent cough, and hurried

shallow respiration of 40 to 48 with temperature of 101 and pulse 100.

The patient was bled 15 ozs. and oxygen added to the air that he

breathed. 'He soon made a complete recovery.

Such venous congestion was more frequent with chlorine poisoning

than it now is with phosgene. It is associated with a full strong pulseat the outset, though later the pulse may fail and the asphyxia change

to the pallid type shown in Plate III. The patient as a rule is fully

conscious and complains chiefly of headache and pains in the chest;he

turns restlessly to and fro in extreme general discomfort, and his

hurried breathing is interrupted from time to time by short bursts of

coughing and of expectoration. The lung is in the oedematous state

shown in Plate I.

Oxygen, when given by an efficient apparatus, will at once change

the blue tint of the face to a full pink colour, showing that it can still

be absorbed by the blood through the lungs. Venesection relieves the

discomfort felt by the patient, and probably lessens the embarrassment

of the circulation.



PLATE II,

\







PLATE NO. Ill

Pallid type of asphyxia from phosgene poisoning, with

circulatory failure.

The cyanotic hue of the ears and lips, despite the general pallor

caused by the failure of the circulation, indicates the intense want of

oxygen from which the patient is suffering. Respiratory difficulty is

shown in the strained effort of the muscles around the nostrils.

History of case. Drawing made on second day after gassing, when

there was profuse frothy expectoration, hurried shallow breathing of

50 a minute and a rapid running pulse of 132. The patient died two

hours later.

This pallid or leaden-hued type of asphyxia is characteristically

frequent after phosgene, and it may either develop at once with a

rapidly progressive failure of the circulation or follow a stage of

venous congestion.

The patient is restless, often semi-delirious, and his skin may be dry

and hot, or cold in the final collapse, though it is not often dampwith perspiration. The hurrying small pulse and the panting rapid

shallow breathing, often with sounds of fluid in the trachea, are bothcharacteristic. Examination of the chest finds physical signs very

similar to those of the blue congested type, a little dulness on per-

cussion and numerous fine rales and rhonchi, especially in the axillae

and over the back. In both cases the intensity of the pulmonary

oedema is hidden from physical examination by the presence every*

where in the lungs of scattered islets of emphysema.



PLATE III







PLATE NO. IV

Gangrene of foot caused by vascular thrombosis from

chlorine poisoning.

History oj case. Gassed by chlorine in 1915 under conditions which

could not have induced frost-bite.

Severe dyspnoea from pulmonaryoedema.

Drawing of foot made on fifth day. Both feet were then anaesthetic,

stone cold, and no pulsation could be felt in the dorsalis pedis artery

The right hand also was mottled, cold, and painful. The circulation

was restored in a few days with complete recovery, except that two

toes beciame black and shrivelled.

Such arterial thrombosis, of slowly progressive onset, is quite

uncommon in the extremities, though it is occasionally seen with

phosgene. The obstruction is very rarely so complete as to cause

gangrene and death of the tissues. But this drawing of a visible

condition is introduced in order to emphasize the fact that an unseen

vascular thrombosis of smaller vessels in deeper organs of the body is

frequently found with phosgene poisoning. Such thrombosis is

.revealed by the microscope in fatal cases in the smaller lung vessels, in

the kidney, in the mucous membrane of the stomach, and in the brain.

Indeed in deaths with

prolonged asphyxiafrom

gassing by phosgenethe white matter of the brain is often seen to be thickly sown with

brownish-red petechial spots around each tiny arterial thrombus. The

obstruction to the lung circulation has already been referred to;the

kidney thrombosis does not appear to have any serious results; and,

except where larger haemorrhages have burst in the brain, the scattered

cerebral thrombi do not appear to be of grave clinical import. The

petechial areas within the stomach may occasionally become the seat

of a superficial ulceration. Large thrombi are sometimes found

within the heart, but they also are associated with rather than the

cause of the other changes that lead to death.



PLATE IV,

i







PLATENO.

VErythema of skin from general exposure to the vapour of

yellow cross substance. Dermatitis of this distribution

and associated with conjunctivitis forms a characteristic

picture of poisoning by this vesicant.

History of case. Exposed to 'mustard gas' at Ypres on July 12,

1917, when this substance was first employed by the enemy. Wore

box respirator for only 30 minutes, so that he was exposed without any

protection for nearly four hours. No symptoms were felt until some

hours later, when severe vomiting commenced and conjunctivitis

developed.

Drawing made on the fifth day. The laryngitis and bronchitis were

slight, so that the poisonous vapour must have acted only in low

concentration. But the reddening of the skin was fairly intense

because the man had been sweating freely when exposed to the gas,

and he was not washed afterwards nor was his

clothing changed.The

erythema was succeeded by staining in the same areas of the skin.

This reddening, as though the skin had been scorched or deeply

sun-burned, is the first cutaneous reaction to mustard gas, though it

sometimes may not appear until several days after exposure. It is

accompanied by only a slight feeling of warmth and irritation. In

addition to the face and arms which are directly exposed to the vapour

in the air, the moist surfaces of the axillae, the flexures of the elbows,

and the perineum and inner surfaces of the thighs are particularly

affected, that is in the places where the skin is often sodden with

fatty perspiration. This special distribution of the diffuse erythema

characterizes the general dermatitis of mustard gas vapour; but the

reaction may be limited to a smaller area in any part of the body, for

example where the clothing may have chanced to be splashed by the

liquid.

The inflammatory reaction is chiefly superficial, and it is not

accompanied by

much oedema of the subcutaneous tissues except in

the eyelids and over the penis and scrotum. Later the dusky red

colour deepens, and patches of cyanotic or whitish oedema may arise

amid it. Blisters then appear, and the cuticle becomes excoriated;or

the skin may be retained while the erythema fades and a brown staining

slowly darkens the original area of irritation.



PLATE V







PLATE NO. VI

Blistering of buttocks by mustard gas.

History of case. The man sat down on ground that was contaminated

by the poison and the vapour passed through his clothing, causing

inflammation of the buttocks and of the scrotum. A diffuse reddening

appeared twenty-four hours after exposure, and this was followed by an

outcrop of superficial blisters. On the eighth day the erythema began

to be replaced by a brown staining, and the drawing was made on the

eleventh day during this change of tints. Infection of the raw surface

was avoided, and the healing was complete in three weeks.

The blisters in this case were probably aggravated by pressure, forthe inflamed skin becomes very fragile, so that the surface layer is

readily loosened by pressure or careless rubbing. The blisters may be

very tiny bullae, as on the eyelids, or they may coalesce into areas

many inches across, covering a collection of serous fluid which perhaps

itself contains enough of the irritant substance to injure other skin if it

is allowed to flow over it.

The blisters are usually quite superficial and almost painless in their

development. But the raw surface that is left after the blister has

burst becomes most acutely sensitive to all forms of mechanical

irritation. Deeper destruction of the dermis may be caused by spread-

ing necrosis where the substance attacks the skin locally in high

concentration, or when secondary infections are implanted on the raw

surface. Chronic and painful sores then result, and in this event the

skin does not regenerate completely, so that thinly covered scars for a

long time will mark the site of the burn.



PLATE VI







PLATE NO. VII

Burning of scrotum and penis by mustard gas.

History of case. From the same incident as that described under

Plate No. VI. Inflammation commenced at the close of the first day

after exposure. Drawing made on the eleventh day when the red

erythema had almost faded from the inner aspects of the thighs. The

scrotum is oedematous and the raw surfaces have become the seat of a

mild secondary eczematisation. The injuries were soon and com-

pletely healed.

The perineum is peculiarly liable to be inflamed after exposure to the

vapour of mustard gas, and the penis and scrotum become oedematous

as well as reddened. Balanitis and pain with micturition may be

troublesome. When the skin is excoriated, secondary infections of the

raw surface are very likely to develop unless adequate precautions are

taken to prevent sepsis. But with careful cleansing of the skin and

clothes of a casualty after exposure to the vapour, inflammation of the

perineum can be reduced to a comparatively trifling incidence.



PLATE VII







PLATE NO. VIII

Brown staining from mustard gas.

This purplish-brown, or brown, or brownish-black tint usually

appears in areas that were first inflamed and red, but it may arise

without such preceding erythema. Its distribution is in the same

areas as those in which erythema occurs, that is over the exposed skin

surfaces of the neck and hands, or on the sheltered moist flexures of

the body. It may appear at any time from the fifth or sixth day

onwards, and it persists for several weeks, until the stained cuticle

desquamates. There is no deep pigmentation.

The drawing was made from a case on the eighteenth day after

exposure to gas, and the brown tint was present on the sixth day.



PLATE VIII,

t

\







PLATE NO. IX

Ulceration of trachea by mustard gas.

The characteristic feature is the sloughing of the tracheal mucous

membrane. The reddening ofthe base of the tongue and ofthe pharynx,with a sharp delimitation where the oesophagus has refused ingress to

the toxic vapour, is seen also with chlorine and other irritant gasses.But the pharyngeal inflammation with mustard gas may proceed

further to a local ulceration that will cause dysphagia for many days.

The mucous membrane of the trachea and bronchi is affected by di-

chlor-ethyl-sulphide in much the same way as is the skin. It reacts

with an intense inflammation, and death of the surface layers soon

results. The mass of necrotic tissue, exuded fibrin, and pus cells mayform a yellowish-grey slough in which all manner of organisms

flourish. Subsequently this false membrane comes away in patches

or in entire casts from the raw surface of the bronchial wall.

Meantime the infected debris and secretions tend to accumulate in

the bronchial ramifications at the bases of the lungs, and infection may

spread from them into the lung tissues and alveoli. Septic broncho-

pneumonia, localised abscesses, superficial pleurisy, and even

empyema or pyopneumothorax then develop and cause death.

The drawing is of a trachea at the twelfth day after gassing. The

base of thetongue and

thepharynx show

characteristic inflammation.

Yellow necrotic sloughs lie on the larynx and at the bifurcation of the

trachea. Between these the trachea is red and glistening, because it

is now completely denuded of both mucous membrane and of slough.

The dotted line points to a little group of ulcers on the posterior wall

from which bleeding has occurred. The trachea and bronchi con-

tained an abundance of thin yellow pus.



PLATE IX







PLATE NO. X

Microscopic section of humanlung

from mustardgas

poisoning, with death at end of second day (40 hours).

The bronchiole is filled with fibrin and pus cells, and its lining

epithelium has been completely destroyed. The inflammation has

caused a characteristic ring of haemorrhage in the tissues around the

bronchial tube, and infection is beginning to appear in the alveoli

nearest to these inflamed tissues. But there is no generalised

pulmonary oedema and no disruptive emphysema.

Di-chlor-ethyl-sulphide may cause some catarrhal desquamation ofthe pulmonary endothelial cells, but it rarely excites an outpouring of

oedema fluid from the pulmonary vessels. The pathological changes

in the bronchioles and in the alveoli are therefore in the sharpest

contrast with those caused by phosgene (see Plate No. I). As

infection spreads into the lung tissues, patches of septic broncho-

pneumonia and small abscesses develop, and these often excite

an inflammatory oedema around them.

If the patient lives, his bronchial mucous membrane is slowly

regenerated ;and during this time he is naturally subject to reflex

spasms of coughing or even to a protracted bronchitis.



PLATE X.







PLATE NO. XlA

Severely burned eye in the acute stage.

Early in the second day after exposure to mustard gas vapour the

eyelids and the external surface of the globe show an intense inflam-

matory reaction. Tears stream from between the closed oedema-

tous eyelids, which may even be blistered, and there is often severe

pain behind the eyes and in the forehead. The conjunctiva is swollen,

oedematous, and bright red from injection of the blood vessels. The

injury of the cornea, even when severe, is not so obvious, and careful

examination is of great importance for its detection. Photophobia and

blepharospasm render examination of the eye very difficult.

The majority of gassed eyes exhibit inflammation of a general

character that is not illustrated in this Atlas. But examples are

continually occurring in which the eye is more severely burned, and

these may be recognized by certain characteristic features that are

depicted in the drawing, Plate No. XI A. Whenever a dead white

band crosses the

exposed

area of the

conjunctiva,

while the

parts

of

this membrane covered by the upper and lower lids are red and

oedematous, serious injury from the burning is likely to have occurred.

In the case illustrated, the caustic effect of the vapour is seen chiefly

in the interpalpebral aperture. On each side of the cornea there is a

dead white band due to coagulative oedema, which compresses the

vessels, impairs the circulation, and thus acts as a menace to the

nutrition of the cornea. The swelling in the region of this white band

is slight, while the protected conjunctiva above and below it is greatly

swollen and injected and may even bulge between the lids.

The exposed portion of the cornea is grey and hazy ;it has lost its

lustre, and when viewed with a bright light and a magnifying glass it

shows a blurred 'window reflex' and a typical 'orange-skinned' surface.

The haze gradually fades off above in the region of the protected

part of the cornea where the surface is usually bright and smooth.

The pupil is at first contracted as the result of irritation and congestion.

In this drawing it is shown as artificially dilated by atropine ointment,

which should always be used early in severe cases or where there is

much pain and blepharospasm.

PLATE NO. X!B

Slightly later stage of acute burning.

The swelling in the conjunctivaabove and belowhas subsided, but the

vascular injection remains, and the solid white oedema in the palpebral

aperture is still well marked. The cornea is grey in the exposedarea.

[For History of the case see pagefacing Plate XII.



PLATE XI.











Plate No. X!B continued.]

History of the case. The casualty was caused by the bursting of a

Yellow Cross shell close to the man when he was riding a restive mule,

and his box respirator was momentarily displaced. A fine spray of

the liquid must have splashed lightly over his right side, for cutaneous

blisters developed on the neck, the cheek, and the forehead on this

side only. The right eye showed serious burning with the central

white band, while the left eye was only in the state of general red

conjunctivitis.

With the lowering of the nutrition of the corneal epithelium,

secondary infection is liable to take place. In this case an infiltrated

corneal ulcer is seen associated with a hypopyon. It is therefore

important when there is conjunctival discharge, which indicates

secondary infection, that in addition to the use of atropine the

conjunctival sac should be cleansed by frequent bland irrigations and

by the instillation of antiseptic drops so as to check infection of any

corneal ulceration which may develop. Otherwise the infective pro-

gress which has led to hypopyon may progress till panophthalmitis

supervenes.

PLATE NO. XIlA

Stage of resolution after severe burning.

The vascular injection is passing off, the solid oedema is becoming

absorbed, and the corneal epithelium has regained its normal lustre,

ki this stage the use of atropine should be discontinued.

PLATE NO. XIlB

Late stage of resolution.

The earlier vascular injection above and below the cornea has

practically disappeared ;the solid white oedema has been absorbed,

and the conjunctiva in the palpebral aperture now shows definite

injection, often of a bright violet tint. The entire picture has changed,

so that the parts which were red in the acute stage are now white and

the part which was formerly white is now red. This drawing would

illustrate equally well the condition that may follow immediately on a

very slight exposure to the irritant gas, when only a slight central bandofred injection develops instead ofthe bloodless state of white oedema

that is caused by the more severe burns.

At this stage atropine and shades should be abandoned. Astringent

drops should be instilled and photophobia combated with cold douching,

&c., while fresh air and occupation will help to restore the general

health of the individual and mitigate any tendency to neurasthenia.



PLATE XII

r







PLATE NO. XIIlA

Drawing of the cornea in the acute stage of severe burning.

This corresponds with Plate No. X!A. The exposed centralarea shows grey haze and loss of lustre on its stippled surface, which

gradually fades off to the bright lustrous normal surface in the part

above that has been protected by the eyelid. Injection of the

conjunctival vessels is seen only in relation to this upper and less

burned area.

PLATE NO. XIIlB

Drawing of cornea in the stage of resolution after severe burning.

The cornea is now smooth and bright with a clear light reflex on

its surface. But some grey superficial nebulae are seen in the centre,

and these may persist for several weeks. The injection of the

conjunctival vessels is now limited to the central band.



PLATE XIII









UG Gt. Brit. National Health

447 Insurance Joint Committee.

G7 Medical Research Committee

An atlas of gas poisoning

PLEASE DO NOT REMOVE

CARDS OR SLIPS FROM THIS POCKET

UNIVERSITY OF TORONTO LIBRARY



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An Atlas of Gas Poisoning UK 1918

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